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SCTR regulates cell cycle-related genes toward anti-proliferation in normal breast cells while having

Seongeun Kang1, Byungtak Kim1, Han-Sung Kang2

  • 1Department of Life Science, Dongguk University-Seoul, Goyang, Republic of Korea.

International Journal of Oncology
|September 24, 2015
PubMed

Insights

Secretin receptor (SCTR) methylation downregulates SCTR in breast cancer, suppressing normal cell growth. However, SCTR overexpression stimulates cancer cell proliferation and migration.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Secretin receptor (SCTR), a G-protein coupled receptor (GPCR), exhibits varied expression in tumors, influencing cancer cell proliferation.
  • The molecular mechanisms behind SCTR dysregulation in cancer remain largely unelucidated.

Purpose of the Study:

  • To investigate the role of SCTR methylation in breast cancer and its impact on cell proliferation and migration.
  • To understand the regulatory mechanisms of SCTR dysregulation in breast cancer.

Main Methods:

  • Methylome database analysis in breast cancer to identify affected pathways.
  • siRNA-mediated downregulation of SCTR in MCF-10A cells followed by pathway analysis.
  • Overexpression of SCTR in MCF-7 cells to assess effects on proliferation and migration.

Main Results:

  • SCTR demonstrated hypermethylation and downregulation in breast cancer tissues (p<0.01 and p<0.05, respectively).
  • Downregulation of SCTR in normal breast cells (MCF-10A) affected the G2/M stage checkpoint and cell cycle genes, suppressing proliferation.
  • SCTR overexpression in breast cancer cells (MCF-7) increased proliferation by 35% and migration by 2.1-fold.

Conclusions:

  • SCTR promoter methylation leads to its downregulation in breast cancer, which suppresses normal breast cell proliferation.
  • Conversely, SCTR stimulates proliferation and migration in breast cancer cells, suggesting a dual role dependent on its expression level and cellular context.

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